DIP Episode 208 - Transfusion Reactions

Okay, welcome. My name is Divine, I'm a resident. This is episode 208 of the Divine Intervention Podcast. And in this podcast, this is going to actually be a short one. I'm going to be talking about transfusion reactions. This is a concept that I am pretty certain of disgusting some other podcasting bits and pieces before. What I just want to have one specifically dedicated to these are reactions because these things are commonly tested on exams. And I feel like I've both treated people recently and just heard from people, many people getting this kind of stuff wrong because they mean they love to test it because it's somewhat confusing and people do not pay much attention to it. So let's just jump right into it. So there are multiple types of transfusion reactions, right? Like there is the acute hemolytic transmission reaction, there is the delayed hemolytic transmission reaction, there is the allergic transmission reaction, there is the fibromone hemolytic transmission reaction, there is something called traly, transmission related acute lung injury, there's something called taco, transmission associated circulatory overload, right? So those are the six major ones that tend to be tested on the USML Es and over the next few minutes I'm going to break those down, explain to you how exactly how they present for an exam so that you can know exactly how they are managed.

So basically the first one, the acute hemolytic transmission reaction, basically the most common cause of this is abu incompatibility. Essentially the thing that happens on MBME exam is these people, right? Let's say for example you're getting type, let's say you're a type O blood person, right? So you have type O blood. So that means you'll have antibodies against the A and T gene and the B antigen, right? So if you've got for a bit for some reason you get A blood or B blood, right? You already have preformed antibodies against those antigen. You get that blood transfusion immediately, you start having hemolysis of those red blood cells with those preformed antibodies and that can cause some pretty significant problems, right? And the most common cause again like I said, a clerical errors, that's a high-oven you want to keep at the back of your mind for these exams. So acute hemolytic transmission reaction, how will you present for an exam? Again, it would be like during the transmission, the patient will start having hematuria, right? The patient will start complying of back pain or flunk pain. So if you see a person during the course of a transmission, complying of flunk pain or back pain and like hematuria, think about an acute hemolytic transmission reaction. And your diagnostic test on an MBME exam is to go ahead and consider performing a direct comp test, okay? A direct comp test. A direct comp test is very, is essentially really diagnostic for for this, right?

And remember that this is actually an example of a type two hypersensitivity reaction, okay? It's an example of a type two hypersensitivity reaction because you have preformed antibodies again, hemolyzing those red blood cells. Those are examples of tides, an example of a type two hypersensitivity reaction. And really in terms of treatment, really what you typically do is you give a ton of fluid, right? By giving that fluid all that hemolysis of red blood cells, so it doesn't gunk up the kidneys and cause like acute tubular macrosis or like an intra-inertic GI. Essentially the thing that happens is that you, you know, you give a ton of fluid, you know, it's almost like the way you filter out the miles is in a sense, right? So you kind of like flush away all that badness. Sometimes people that have these acute hemolytic transmission reactions, they go into DIC. Under those circumstances, you know, you want to give them like platelets, you want to give them like cryoprecipitate, you want to give them FFP. But other than that, that's pretty much how you manage, that's pretty much how you manage those disorders, right? So again, the most common cause is a clerical error. Again, that's something absolutely wants to come into memory. And again, red urine, right? So hematuria, like hemoglobinuria, right? And you have flunk pain. That's what you're looking for on an in-be-mixer. Now, a delayed hemolytic transmission reaction.

Basically, the pathophysiology is essentially the same thing as an acute hemolytic transmission reaction. But the reaction does not, the key difference is that the reaction does not occur during the transmission. It would usually occur like days after the transmission has happened. That's the classic thing that you tend to put on in-be-mixers, okay? So the problem arises days after the transmission has happened. And they will typically in that case, they give you like a cum stress result and you will actually notice that you'll be positive, right? So those people will have a positive direct cum stress, but they will have again a hemolytic episode days after the transmission happened. And the key critical thing there is that those people tend to have much less severe reactions. They didn't have much less severe reactions, right? So they usually do not, you know, it's not something that requires like organbusters, ribbons or anything like that. The reactions are usually pretty, pretty, pretty mild, right? So it's also a kind of type two hypersensitivity reaction. And again, it happens days after the transmission happens. And usually it typically does not arise because of ebueing compatibility. It almost always arises because of some other kind of antigen like the kid antigen like the GI, double the antigen or the, sometimes you can see like the Kell antigen or the doffy antigen. Those are kind of like the big things there.

So that's all I think I'm going to say about the late hemolytic transmission reaction. Now, the next one I think I want to jump to is the allergic transmission reaction. This classically shows open MB Ms in the context of a pressing that has IG deficiency. Essentially, the thing that happens is you, you get a blood transfusion and when you get a blood transfusion, they ask you that, that transfused blood contains things that you have IGE antibodies against, right? Contains things you have IGE antibodies against. So if you take that transfused blood, you take those antigens from those antigens, you know, they will react with IGE. You have cross-linking of the, you have cross-linking of the, of the IG Es on the surfaces of mast cells, right? When you release those nasty things like histamine and heparin and all that stuff and that can cause bronchospasem and cause pretty significant problems, right? So those people, the classic presentation, the airway problems, okay? They will have predominantly airway problems, right? So they'll have like bronchospasem, they'll have wheezing, right?

They'll have like an anaphylactic stout presentation and typically the thing you do for those people, I mean if it's a mild reaction, if like they're satin-fine, their blood pressure is fine and everything, you can go ahead and give those people an antihistamine and then you know, if they kind of get better, you can then resume the reaction, but if it's like a severe reaction, which I would say for the most part, you should maybe expect more on an in-beam exam. You want to go ahead and give those people IMEP in effort because it's literally an anaphylactic reaction, right? And because it's an anaphylactic reaction or you can say an allergic reaction, essentially the thing that's happening with those foxes is it's, it's actually a type one hypersensitivity reaction. That's one thing the in-beam kind of expect you to know, it's a type one hypersensitivity reaction and think about it, right? Think about this. People that are IgE deficient, right? If they IgE is a foreign local to them, right? So if for example they get transfused blood and that transfused blood contains IgE, right? Then they probably have like IgE antibodies because remember, you know when you get exposed to an allergic or an antigen the first time the first antibody you make is IgM, but after you make IgM there is such a thing as claspswiching, right? And claspswiching, especially if you're looking using interlooking four, you can claspswich to IgG and IgE.

Or if you have interlooking five you can claspswich to IgE, right? So the thing is if you make IgE antibodies then you begin to get into trouble, right? And you can get those kinds of problems. And again because it's an anaphylactic reaction, for the most part you need to strongly consider putting those people on an IMA pinnephrase, right? So that they don't pass away. Now the next one I want to talk about, I want to talk about the febrile non-hebolytic transition reaction, okay? The febrile non-hebolytic transition reaction. Essentially the febrile non-hebolytic transition reaction pretty much can arise by the way it will present is typically will be a person that during the course of a blood transfusion they develop like fevers, right? But you know they'll be febrile, they may have like a mild tacky cardia, but they won't really have significant hemodynamic instability, okay? They won't really have significant hemodynamic instability. And one key thing to keep at the back of your mind with these are febrile reactions, right? Is again either during the transfusion or you know around like one to four hours after the transfusion is over, okay? That's one thing you absolutely want to keep at the back of your mind on exams, right?

And the thing is this is actually one of those things where understanding the mechanism is very useful for purposes of the NV Me exams because the thing is your friends at the NV Me they begin to write these questions where they demand mechanistic reasoning, especially on step two CK. I mean step one they've been doing it all along, right? But step two CK, right? So one thing I will definitely say is it's probably not the worst idea in the world to understand this. And the reason that I'm going to emphasize the mechanism here today is that there are some very nice parallels with the mechanism behind another kind of transfusion reaction called trolley. Transfusion released it acute lung injury, right? So let's go ahead and break that down and talk about things, right? So the thing is when a person has a febrile monhemolytic transfusion reaction, the thing that happens is they are one of two mechanisms. Let me talk about the easy mechanism and then I'll talk about the hard mechanism. The easy mechanism, which is the first one, essentially revolves around the fact that when you have blood elements, right? Especially platelets, platelets are probably one of the big ones that tend to cause this kind of problem, right? Blood, when you know, you have blood stored in the blood bank, it can actually contain white blood cells and those white blood cells, right? Especially again, the reason I'm saying it's platelets is white blood cells, they survive very well at room temperature.

The thing is platelets tend to generally be stored at room temperature, most other blood elements and not stored at room temperature. So the thing that happens is if you have platelets, you know, you get a platelet transfusion and then from those platelet transfusions, you, you, those white blood cells that have been sitting in the blood bank, you know, they are still active, they are still able to make cytokines, those cytokines, right? Can, you know, activate, like, you know, cause fever and all that stuff, right? So you know, the person will have like fever, chill, some maltaqi cardio, nothing serious there. All you need to do for these people is just give them something that reduces fever like, you can give like a set of minofin, for example, right? And again, these transfusion reactions, I promise you like on many shelf exams, like surgery, medicine, peds, they love to test all this stuff. So this is something you absolutely want to make sure you understand and keep at the back of your mind, for example, it's just something that they love, love, love, love, love to test all the time on tests. So that's the easy mechanism. The heart mechanism is that for a febrile non-hymolytic transfusion reaction, the thing that happens is you can have antibodies. So the person rate, the recipient of the blood transfusion, right? The recipient has antibodies and those antibodies, they can attack white blood cells that are present.

They can attack white blood cells that are present on the in the blood that's been transfused, right? And basically the thing that happens is you essentially form an antigen antibody complex. So this is actually an example of a type three hypersensitivity reaction. So you form an antigen antibody complex. And the thing is when those antibodies, right, from the from the recipient bind to the antigens, which are the leukocytes of the donor blood, right? You then have a release of cytokines and then that causes all those problems, right? So the reason I'm being very specific here is that in a febrile non-hymolytic transfusion reaction, I'm saying that the antibodies come from the recipient and then the antigens on the white blood cells are in the donor blood. That is very different from what obtains in trily transfusion relief rate acute lung injury, okay? You have the antibodies coming from the donor blood and then you have the affected leukocytes coming from the recipient's blood, okay? So that's something you absolutely want to keep at the back of your mind, for example, right? So I guess with that said, let me just maybe go ahead and jump to the transfusion related acute lung injury. The easy way to understand transfusion related acute lung injuries, this is essentially ARDS in a person that gets a blood transfusion. That is literally the easiest way to think about this. It's ARDS in a person that gets a blood transfusion. And again, I essentially already explained, right?

You have antibodies in the donor blood attacking white blood cells in the recipient blood. And when you have that, again, antigen antibody complex come together. So again, that'll be an example of a type three hypersensitivity reaction. You can release things like histamine, for example, you can release really kind, you can release leukotrines. Remember, those things, especially, especially if you have like an antigen, one antigen antibody complex that has a greater affinity for the lung parankoma, those things can settle there. And all that inflammation that then happens will subsequently cause like long damage. You'll increase pulmonary vasculopremability and you have essentially like a non-cardiogenic pulmonary dima. In fact, I can envision your friends at the MBM, right in a question where they give you a pulmonary capillary which preserves a person that has trally. And obviously that pulmonary capillary which preserves will be normal. You'll be less than the magic number of 18, okay? You'll be less than the magic number of 18, right? Because the person has a non-cardiogenic pulmonary dima. That is something you absolutely want to commit to memory for your exams, okay? Now, the thing is, you may see it divine. Can you maybe give me an analogy that may help you understand this? The thing is, think about it. Think about it. When a person has like one of these nephrodic and ephrodic syndrome, so we all know that it arises from antigen-antibody complexes.

Those antigen-antibody complexes, they go to the kidneys. You know, like some people that you know just when they come to a place, trouble comes with them, right? It's kind of like the same thing. You have these antigen-antibody complex, they are like, oh, they may have been from somewhere completely different. And then they say, oh, you know, let's come to the kidney. Maybe because they have like very good affinity for some kidney antigens, they come there and they trigger chaos and then they destroy the kidneys, right? So I almost think of trally. Like if you really dig down to the pathophysiology, the pathophysiology is almost identical to what happens in the kidneys. It's almost like like one of those nephrodic and ephrodic syndromes, but it happens in the lungs because those antigens and antibodies, the antigen-antibody complexes settle in the lungs instead of settling in the kidneys, okay? So that's the mechanism. That's the pathophysiology behind transfusion related acute lung injury, okay? Transfusion related acute lung injury. That's again, that's a high-youth thing to know. And again, it's essentially like ARDS. So essentially what you want to do for these people is you know, you want to give them like pulmonary support. Trial, it has a pretty high mortality, you know, just, you know, pulmonary support is going to be placed on vents. You can give them like, if they have high potency, if you can give them fluids, you can give them pressures.

It's actually very high-youth remember that you don't want to give these people diuretics. Diuretics are a terrible idea in a person that in a person that has a transfusion related acute lung injury. In some cases, you could also give these people clinical steroids. So just kind of know those different treatments for travi. Now, the other transfusion related reaction I think I want to talk about is taco, right? So transfusion associated a secretary overload. Basically, this one is almost like, this one is essentially like a person that has like risk factors for like, you know, like bad hearts, you know, like heart failure, blah, blah, blah, blah, blah, you give them like a large volume blood transfusion, right? And then they subsequently get into trouble because their hearts cannot handle the fluid. So because your hearts cannot handle the fluid, most of that fluid, the blood from the large volume transfusion kind of backs up in the lungs. And if you backs up in the lungs, that's a problem, right? Because that was cause-pobonary dima. But unlike Charlie, which I said was a non-cardiogenic pomonary dima taco is a cardiogenic pomonary dima, okay? So in this circumstance, the pomonary capillary which pressure will be greater than the magic number of 18. And because this is essentially almost like a fluid overload, right? Then treatment will, it would make sense that giving diuretics helps significantly on that these are circumstances.

And one other thing that your friends at the end in me do to, you know, mildly mess with your head is, if a person has a taco, right? Like they may give you like a B and they can give you, I can just imagine them giving you like a chart with arrows. And then they put like the PCWP in one hour, they put like the central venous pressure in one hour, they put like the BMP writing one hour. And all those things will go up, right? Remember the CVP is a proxy for right? It's your pressure. You will go up because there's fluid overload in the hearts. The heart cannot come that lot forward, right? And then the PCWP, which is a surrogate for left H.O. pressure will also be increased, right? And obviously, right, the presence BMP will be increased because remember whenever the chambers of the H.R. or the ventricles are distended with fluid, right? Especially like on a chronic basis, they tend to release a ton of, they tend to release a ton of AMP and BMP to try to counter those effects, basically like to almost like shut down the activity of the reading and the testing on the student system. So you can get rid of that excess of that excess fluid. So that's the pathophysiology and that's the treatment for for taco, right? Now, another thing I want to talk about in terms of, um, um, transmission reactions, right? So there's this thing known as a transmission associated graft versus host disease. Transfusion associated graft versus host disease, I mean, it's very bad.

The mortality is, uh, the mortality is terrible. Basically, the thing that happens is that you have T cells in the donor blood, they begin to attack, like T-shoe in the recipe, like in the recipe, right? That's obviously like super, super, super, super bad, right? That is super, super, super bad. I mean, if I'm long-nesticking, the mortality for this is like 90% or like some really high, I'm pretty sure it's at least 90%. Right? So it's pretty bad, right? And usually the risk factor is the recipe, it may be like an immunocompromised person, maybe this person recently got like a like a bone marrow transplant or something like that. And typically those people, you know, after they get the transmission, they'll begin to have fevers, they'll have like a rash. Sometimes they can have like big liver, right? So they have like a pato megalith, they can have diarrhea, they can have like a panside opine, like all the, like their white blood cell, count red blood cell, completely count everything will be low. Just, you know, just badness all around, just badness, badness, badness all around. And you may say, okay, how do you prevent this? Well, the way you prevent this is you use gamma risk to essentially irreduce the person's blood. I mean, it radiates the donor blood, right? So that you don't get into those problems so that the T cells are killed and destroyed. I mean, basically on an MDM exam, you want to think twice and better know what you're doing.

And also in the real world, before giving blood transfusions to immunocompromised patients, because things like this can happen. And again, transfigure and associated graft versus host disease, there's literally no treatment. The person is almost certainly going to die, right? So you just want to keep those things at the back of your mind. And then one thing I think I want to mention is this whole idea of a local reduction. Local reduction is basically where you try to reduce the number of white blood cells in a donor blood sample. That thing can actually help quite significantly with, with a graft, I mean, not with the fibromonti-molelic transition reaction, because essentially getting rid of the white blood cells that can produce those cytokines and give rise to trouble, right? And local reduction, right? It's also, again, something you can do, something you can do if a mum is speaking, also in people that have had like allergic transfusion reactions, but that I'm not 100% sure of how I'd encourage you to look that up, but I'm fairly setting that issue. So I think I've pretty much discussed all the major high-yield ones. So I think I'm going to go ahead and pause here. As I do at the end of every podcast, I do offer one on one tutoring for many exams and also a large group tutoring for the USM list, step one, step two CK, step three, step two CS exams, pre-clinical medical exams, right? Third year shelf exams, basically all the shelf exams I tutor for.

And then if you're a college student applying to med school, so like an ERAS application, I mean an AMCA application or a med student applying to residency, so like an ERAS application I do offer, again like one on one coaching with like rec letters, personal editing, personal statements, editing applications, doing work interviews. Again, I've worked with tons of people and the vast majority of people have worked with, have all much that they are first choice. And then I offer these booster courses for step one, step two CK and step three, where it's 15 hours for step two CK and step three and it's 10 hour, I mean it's 20 hours for step one. And the long and short of things is I essentially review the most known the high yields for those exams in a very short time frame. I meet with the Tuti over a couple of sessions. And again, many people that have done that with a founded to be extremely helpful. And so if you need details on email these things, just reach out to me that through the website or you can send me an email, divine intervention podcasts with an sdn.gmail.com. Right? And then if you know, no, a college body that needs to bring from a general chemistry, organic chemistry, physics, biochemistry, histology, physiology, again, I do offer one on one tutoring for all those students. So have a wonderful night rest. Thank you for listening to this podcast. Please subscribe to the website. Please subscribe.

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Clerical error, specifically ABO incompatibility.

AHTR occurs immediately/during transfusion; DHTR occurs days after transfusion.

Type I Hypersensitivity (IgE mediated).

Transfusion Related Acute Lung Injury (TRALI).

TACO has elevated PCWP (>18 mm Hg); TRALI has normal/low PCWP.

Cytokine release from stored white blood cells activated by platelet transfusions, causing fever.

Type II Hypersensitivity; preformed antibodies attack donor RB Cs.

Positive Indirect Coombs Test (IAT) days after transfusion.

Intramuscular Epinephrine (IM Epi).

TRALI (Transfusion Related Acute Lung Injury).

Using Gamma globulin to inactivate T cells.

Both will be elevated (>18 mm Hg) due to fluid overload/heart failure.

Type II Hypersensitivity; preformed antibodies attack donor RB Cs.

Positive Indirect Coombs Test (IAT) days after transfusion.

Intramuscular Epinephrine (IM Epi).

TRALI (Transfusion Related Acute Lung Injury).

Using Gamma globulin to inactivate T cells.

Both will be elevated (>18 mm Hg) due to fluid overload/heart failure.